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Tytuł pozycji:

Connexin36 contributes to INS-1E cells survival through modulation of cytokine-induced oxidative stress, ER stress and AMPK activity.

Tytuł :
Connexin36 contributes to INS-1E cells survival through modulation of cytokine-induced oxidative stress, ER stress and AMPK activity.
Index Terms :
Sciences bio-médicales et agricoles
AMP-Activated Protein Kinases -- metabolism
Animals
Apoptosis -- drug effects
Calcium -- metabolism
Caspase 3 -- metabolism
Cell Survival -- drug effects
Connexins -- genetics -- metabolism
Cyclic AMP -- metabolism
Cytokines -- pharmacology
Down-Regulation -- drug effects
Endoplasmic Reticulum Stress -- drug effects
Feedback, Physiological -- drug effects
Humans
Insulin -- biosynthesis
Insulin-Secreting Cells -- drug effects -- metabolism -- pathology
Interleukin-1beta -- pharmacology
Metformin -- pharmacology
Mice
Mitochondria -- drug effects -- metabolism
Models, Biological
Oxidative Stress -- drug effects
Rats
Reactive Nitrogen Species -- metabolism
Reactive Oxygen Species -- metabolism
Response Elements -- genetics
Transcription, Genetic -- drug effects
info:eu-repo/semantics/article
info:ulb-repo/semantics/articlePeerReview
info:ulb-repo/semantics/openurl/article
Wydawca :
2013-12
Dodane szczegóły :
Allagnat, Florent
Klee, Philippe
Cardozo, Alessandra K
Meda, P
Haefliger, J A
Typ dokumentu :
Zasób elektroniczny
URL :
http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/164672">http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/164672
http://worldcat.org/search?q=on:EQY+http://difusion-oai.ulb.ac.be/oai/request+DCG_ENTIRE_REPOSITORY+CNTCOLL">http://worldcat.org/search?q=on:EQY+http://difusion-oai.ulb.ac.be/oai/request+DCG_ENTIRE_REPOSITORY+CNTCOLL
Dostępność :
Open access content. Open access content
1 full-text file(s): info:eu-repo/semantics/restrictedAccess
Pozostałe numery :
EQY oai:dipot.ulb.ac.be:2013/164672
893984089
Źródło wspomagające :
UNIV LIBR DE BRUXELLES
From OAIster®, provided by the OCLC Cooperative.
Numer akcesji :
edsoai.ocn893984089
Zasób elektroniczny
Cell-to-cell communication mediated by gap junctions made of Connexin36 (Cx36) contributes to pancreatic β-cell function. We have recently demonstrated that Cx36 also supports β-cell survival by a still unclear mechanism. Using specific Cx36 siRNAs or adenoviral vectors, we now show that Cx36 downregulation promotes apoptosis in INS-1E cells exposed to the pro-inflammatory cytokines (IL-1β, TNF-α and IFN-γ) involved at the onset of type 1 diabetes, whereas Cx36 overexpression protects against this effect. Cx36 overexpression also protects INS-1E cells against endoplasmic reticulum (ER) stress-mediated apoptosis, and alleviates the cytokine-induced production of reactive oxygen species, the depletion of the ER Ca(2+) stores, the CHOP overexpression and the degradation of the anti-apoptotic protein Bcl-2 and Mcl-1. We further show that cytokines activate the AMP-dependent protein kinase (AMPK) in a NO-dependent and ER-stress-dependent manner and that AMPK inhibits Cx36 expression. Altogether, the data suggest that Cx36 is involved in Ca(2+) homeostasis within the ER and that Cx36 expression is downregulated following ER stress and subsequent AMPK activation. As a result, cytokine-induced Cx36 downregulation elicits a positive feedback loop that amplifies ER stress and AMPK activation, leading to further Cx36 downregulation. The data reveal that Cx36 plays a central role in the oxidative stress and ER stress induced by cytokines and the subsequent regulation of AMPK activity, which in turn controls Cx36 expression and mitochondria-dependent apoptosis of insulin-producing cells.
Journal Article
Research Support, N.I.H. Extramural
Research Support, Non-U.S. Gov't
SCOPUS: ar.j
info:eu-repo/semantics/published

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